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Thread: Molecules and aging

  1. #1 Molecules and aging 
    Forum Sophomore Dkav's Avatar
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    Do molecules in animals such as DNA age and what happens during the process? Would saying they have a half life be more appropriate?


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  3. #2  
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    Found this on a wiki page:

    Cellular senescence is the phenomenon by which normal diploid cells lose the ability to divide, normally after about 50 cell divisions in vitro. Some cells become senescent after fewer replications cycles as a result of DNA double strand breaks, toxins, etc. This phenomenon is also known as "replicative senescence", the "Hayflick phenomenon", or the Hayflick limit in honour of Dr. Leonard Hayflick who was the first to publish this information in 1965. In response to DNA damage (including shortened telomeres), cells either age or self-destruct (apoptosis, programmed cell death) if the damage cannot be easily repaired.

    http://en.wikipedia.org/wiki/Senescence


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    Forum Sophomore Dkav's Avatar
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    Quote Originally Posted by fatman57
    Found this on a wiki page:

    Cellular senescence is the phenomenon by which normal diploid cells lose the ability to divide, normally after about 50 cell divisions in vitro. Some cells become senescent after fewer replications cycles as a result of DNA double strand breaks, toxins, etc. This phenomenon is also known as "replicative senescence", the "Hayflick phenomenon", or the Hayflick limit in honour of Dr. Leonard Hayflick who was the first to publish this information in 1965. In response to DNA damage (including shortened telomeres), cells either age or self-destruct (apoptosis, programmed cell death) if the damage cannot be easily repaired.

    http://en.wikipedia.org/wiki/Senescence
    I'm talking about molecules. So if you put DNA in a test-tube with an environment like the human body, what changes would the DNA undergo with age and how/why?
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    the primary damage done to DNA is oxidative damage done by reactive oxygen species. Detection of significant oxidative damage such as this is also a trigger for apoptosis or PCD.

    both detection of this type of damage or other types of damage as mentioned by fatman cause cell death because without this mechanism cells with significantly damaged DNA will reproduce, which is not reproductively sound for a multicellular organism or even single celled organisms.
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  6. #5  
    Forum Sophomore Dkav's Avatar
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    Sorry for the late reply. Let me rephrase. What is Dr.Hayflick talking about when he says "the biology of old molecules provides the ground for the emergence of age associated diseases" in this 1 min. clip on youtube http://www.youtube.com/watch?v=tBeNdzCTqck
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    the answer remains the same. over time many of the chemicals associated with biology are oxidized. reactive oxygen species can create mutations or degradations in the DNA and RNA. DNA damage of course being quite dangerous to the cell. excess DNA damage can lead to cancerous or otherwise abnormal cells, or as earlier mentioned can cause PCD.

    another class of molecules that may undergo significant damage over time is proteins. unfortunately my knowledge of protein proofreading within the cell is basically absent however the DNA is continually checked for changes which are either repaired or otherwise eliminated, after proofreading only about one in a million of the changes to a cell's DNA remain. proteins on the other hand may go largely unchecked and after a large amount of time functioning in the cell may be degraded into an inactive form or gain new properties which were previously not associated with that protein.

    zooming out these changes in proteins and other molecules cause the sagging of the skin, decreased mental function, changed physiological norms, and accursed grey hair associated with aging.
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    what the hell is he talking about then when he says "that area has been entirely neglected"?????
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  9. #8  
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    Proteins can be marked for recycling by chaperone proteins and others (also known as heat shock proteins because they were discovered by their upregulation during periods of "shcoking" bacterial cells). They can sometimes refold proteins that get denatured, but often the cell frequently breaks down proteins and simply makes new ones. This can go wrong of course, which is when you get things like prions or build ups of damaging proteins like in Alzheimer's. The mechanisms are complicated and poorly understood, mostly it has to do with recognizing a.a. sequences that should not be accessible on the surface of proteins.

    As to DNA, it's important to recognize that there are DNA repair mechanisms, that try to detect anomalies and prevent the build up of mutations. You also have apoptosis as a line of defense against cells with damaged genomes. Then after apoptosis you've got the immune system on the look out for odd cells. When all those backups fail you end up with something nasty like cancer.
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  10. #9  
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    Quote Originally Posted by i_feel_tiredsleepy
    Proteins can be marked for recycling by chaperone proteins and others (also known as heat shock proteins because they were discovered by their upregulation during periods of "shcoking" bacterial cells). They can sometimes refold proteins that get denatured, but often the cell frequently breaks down proteins and simply makes new ones. This can go wrong of course, which is when you get things like prions or build ups of damaging proteins like in Alzheimer's. The mechanisms are complicated and poorly understood, mostly it has to do with recognizing a.a. sequences that should not be accessible on the surface of proteins.

    As to DNA, it's important to recognize that there are DNA repair mechanisms, that try to detect anomalies and prevent the build up of mutations. You also have apoptosis as a line of defense against cells with damaged genomes. Then after apoptosis you've got the immune system on the look out for odd cells. When all those backups fail you end up with something nasty like cancer.
    Marked for recycling via ubiquitination?
    what do you mean by recognizing a.a sequences that should not be accessible on the surface of proteins?
    accessible by whom?...by dna polymerase?
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  11. #10  
    Forum Cosmic Wizard i_feel_tiredsleepy's Avatar
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    Quote Originally Posted by Dkav
    Marked for recycling via ubiquitination?
    I'm a microbiologist so I'm more used to prokaryotes that don't have ubiquitone. However, my understanding is that they do the tagging in eukaryotes to bring them to the proteasome. I think E3 proteins and hsp proteins are the ones involved specifically in choosing which ones will be tagged by the ubiquitin. This is like way out of my comfort zone in biochem though. Hsp seem to try to refold a protein before it gets targeted for degradation.

    what do you mean by recognizing a.a sequences that should not be accessible on the surface of proteins?
    By the proteins involved with the targetting for degradation, I'm not sure how much is known. I also know that the terminal sequence of the amino acid plays a major role in determining the half-life. I recall reading about proteins recognizing domains and residues that are normally folded inwards in proteins. I found this example of an E3 ubiquitin-ligase recognizing the transmembrane domain of a protein.

    http://www.cell.com/molecular-cell/a...2809%2900200-7
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  12. #11  
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    siiick. Thank you.
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